Grøndahl M L, Jensen G M, Nielsen C G, Skadhauge E, Olsen J E, Hansen M B
Department of Physiology, Royal Veterinary and Agricultural University, Frederiksberg C, Denmark.
J Med Microbiol. 1998 Feb;47(2):151-7. doi: 10.1099/00222615-47-2-151.
The involvement of 5-hydroxytryptamine (5-HT) and 5-HT3 receptors and prostaglandin E2 (PGE2) in Salmonella Typhimurium-induced fluid accumulation in the porcine small intestine was investigated. Salmonella Typhimurium (10(8) and 10(10) cfu) and cholera toxin (CT; 20 microg) were instilled for 8 and 11 h in ligated loops in the porcine jejunum and ileum. Fluid accumulation and concentrations of Na+, K+, Cl-, 5-HT and PGE2 in the fluid accumulated in the loops were measured. The fluid accumulation was also measured when Salmonella Typhimurium (10(10) cfu) and CT (20 microg) were instilled for 8 h in ligated loops in jejunum and ileum in pigs given subcutaneous injections of saline or the 5-HT3 receptor antagonist ondansetron (200 microg/kg). Salmonella Typhimurium (10(10) cfu) and CT both induced fluid accumulation in jejunum and ileum after 8 and 11 h. Both treatments also induced an increase in luminal release of 5-HT and PGE2. The accumulated fluid was iso-osmotic and hyperosmotic in CT- and Salmonella Typhimurium-treated loops, respectively. Ondansetron reduced the Typhimurium-induced fluid accumulation in both jejunum and ileum by c. 40%, while it failed to reduce the response to CT. These results demonstrate that 5-HT and PGE2 are released and 5-HT3 receptors activated in the secretory pathway of Typhimurium in the porcine small intestine.
研究了5-羟色胺(5-HT)及其5-HT3受体以及前列腺素E2(PGE2)在鼠伤寒沙门氏菌诱导的猪小肠液体蓄积中的作用。将鼠伤寒沙门氏菌(10⁸和10¹⁰ cfu)和霍乱毒素(CT;20微克)注入猪空肠和回肠的结扎肠袢中8小时和11小时。测量肠袢中蓄积液体的液体蓄积量以及Na⁺、K⁺、Cl⁻、5-HT和PGE2的浓度。当给猪皮下注射生理盐水或5-HT3受体拮抗剂昂丹司琼(200微克/千克)后,将鼠伤寒沙门氏菌(10¹⁰ cfu)和CT(20微克)注入空肠和回肠的结扎肠袢中8小时,也测量液体蓄积量。8小时和11小时后,鼠伤寒沙门氏菌(10¹⁰ cfu)和CT均诱导空肠和回肠出现液体蓄积。两种处理还均诱导肠腔内5-HT和PGE2释放增加。在CT处理组和鼠伤寒沙门氏菌处理组的肠袢中,蓄积的液体分别为等渗和高渗。昂丹司琼使鼠伤寒沙门氏菌诱导的空肠和回肠液体蓄积减少约40%,而未能降低对CT的反应。这些结果表明,在猪小肠中,鼠伤寒沙门氏菌的分泌途径中释放了5-HT和PGE2并激活了5-HT3受体。